Tissue fibrosis is a condition characterized by an abnormal accumulation of extracellular matrix and inflammatory factors that result in scarring and promote chronic organ injury. In liver, fibrosis is a multi-cellular response to hepatic injury that can lead to cirrhosis and hepatocellular cancer. The response is often triggered by liver injury associated with conditions such as alcohol abuse, viral hepatitis, metabolic diseases, and liver diseases, such as a cholestatic liver disease, nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH). Studies have implicated high mobility group box 1 (HMGB1) protein as having a pro-fibrotic role in liver fibrosis. (See, e.g., Li L-C, et al., Emerging role of HMGB1 in fibrotic diseases, J. Cell. Mol. Med. Vol 18, No 12, 2014 pp. 2331-2339) HMGB1 is a nuclear protein released from injured cells that functions as a proinflammatory mediator and has been shown to recruit hepatic stellate cells and liver endothelial cells to sites of liver injury. (Seo, Y S, et al., HMGB1 recruits hepatic stellate cells and liver endothelial cells to sites of ethanol-induced parenchymal cell injury, Am J Physiol Gastrointest Liver Physiol 305: G838-G848, 2013.) Hepatic stellate cells are believed to play a central role in the progression of liver fibrosis through their transformation into proliferative myofibroblastic cells that promote fibrogenic activity in the liver. (See, Kao Y H, et al. High-mobility group box 1 protein activates hepatic stellate cells in vitro. Transplant Proc. 2008; 40: 2704-5)